NTRK1 and infection: Endosomal proteases play an essential role in EBOV infection following its host cell entry. By designing antagonists to these enzymes, EBOV trafficking, maturation and infection can be averted. Moreover the clathrin-dependent endocytosis with evident roles of NPC1 receptor, GP proteins, TIM-1, TIM-4, and Axl (a receptor tyrosine kinase) for entry of enveloped EBOV provides essential information for designing entry inhibitors against EBOV. These proteins are targeted and blocked in different methods to design particular viral entry inhibitor drugs. [27,29,30]